Journal of Leukocyte Biology
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A more recent version of this article appeared on August 1, 2006

Published online before print May 30, 2006
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0406245

Received for publication April 5, 2006.

Accepted for publication April 25, 2006.

Article

Hypothesis: the antitumor activities of statins may be mediated by IL-18

Hideo Kohka Takahashi *, Gabriele Weitz-Schmidt {dagger}, Hiromi Iwagaki {ddagger}, Tadashi Yoshino {sect}, Noriaki Tanaka {ddagger}, and Masahiro Nishibori *@

Departments of *Pharmacology, {ddagger}Gastroenterological Surgery, Transplant, and Surgical Oncology, and {sect}Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Japan; and {dagger}Novartis Institutes for Biomedical Research, Basel, Switzerland

@ To whom correspondence should be addressed. E-mail: mbori{at}md.okayama-u.ac.jp.


  Abstract

Statins, which inhibit 3-hydroxy-3-methylglutaryl coenzyme-A (HMG-CoA) reductase, are thought to reduce the risk of cancer through the inhibition of Ras farnesylation and serum lipid level. A pleiotropic proinflammatory cytokine, interleukin-18 (IL-18), is reported to exhibit significant antitumor activities through the activation of cytotoxic T lymphocytes and natural killer cells and the inhibition of angiogenesis. Previously, we found that pravastatin, fluvastatin, and simvastatin induced the production of IL-18 in human monocytes. The addition of mevalonate abolished the IL-18 production induced by pravastatin, fluvastatin, and simvastatin, indicating that the IL-18 production might be a result of the inhibition of HMG-CoA reductase. We present a new hypothesis that the production of IL-18 might play roles in the action of statins on cancer.

Key Words: statin • cancer






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